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Identifying novel genes in these pathways can potentially lead to new osteoporosis therapies.
Thus, propagation of the pathology via neural pathways can potentially explain how α-syn aggregates spread in PD.
For instance alteration of components of MAPK, NF-k-B and apoptosis pathways can potentially affect other cellular phenomena such as angiogenesis.
Hence, both calcineurin-dependent and calcineurin-independent pathways can potentially mediate the CsA-mediated survival of NPCs observed in vitro and in vivo.
It was emphasized that these two pathways can potentially be distinguished by transient kinetic measurements, and that, for a given complex, both mechanisms may be operational, with the preferred reaction path being modulated by the protein and ligand concentrations.
Our results indicate that the activation of compensatory pathways can potentially cause up-regulation of EGFR/ErbB pathway genes (counteracting the inhibiting effect of lapatinib) via signaling cross-talk.
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Therefore while inhibition of Ras/MAPK pathway can potentially enhance TIL numbers by enhancing tumor immunogenicity15, theoretically it likely simultaneously inhibits effector T-cell function21,22,23,24,25, though the clinical relevance of this is currently unclear.
However, interfering with the NF-κB pathway can potentially lead to numerous adverse effects.
Receptors internalized in either pathway can potentially be recycled, or degraded.
To explore to what extent the BMP signalling pathway can potentially be activated by BMP ligands, we assessed the levels of BMP ligand expression at the invasive front.
A mutation in any component of the miRNA processing pathway can potentially modify the expression of miRNAs, causing dysregulation of their target mRNA expression.
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